Electroconvulsive Therapy

Author: Raj K Kalapatapu, MD; Chief Editor: Dennis M Popeo, MD more...

Updated: Jan 12, 2015

Overview
Introduction

Electroconvulsive therapy (ECT) has been demonstrated to be an effective and safe

treatment for many psychiatric disorders. [1] The use of ECT still generates
significant controversy, however. One review concluded that ECT is only marginally
more effective than placebo (ie, sham ECT). [2] ECT has been viewed as harmful by
the general public, [3] psychiatric patients, [4] and mental health professionals. [5]

ECT has also been perceived as a form of violence against women. [6] It has been
negatively portrayed in movies such as One Flew Over the Cuckoo's Nest, House on
Haunted Hill, and Requiem for a Dream. [7]

Help your patients with insomnia

fall asleep faster Start here
Information from Industry
Despite such debate, ECT is used in the United States and endorsed by the
American Psychiatric Association. [8] Approximately 100,000 patients annually
receive ECT in the United States. [9] Professional associations in Austria, Canada,
Australia, Denmark, Netherlands, Germany, and India have offered professional
guidelines for its use. [10]

The image below depicts electroconvulsive therapy.

Electroconvulsive therapy (ECT) can help some people with bipolar disorder. ECT uses an
electric current to cause a seizure in the brain and is one of the fastest ways to ease severe
symptoms. It is usually a last resort when a patient does not improve with medication or
psychotherapy.

History

In the 1500s, the Swiss physician Paracelsus (Auroleus Phillipus Theostratus

Bombastus von Hohenheim) induced seizures by administering camphor by mouth
to treat psychiatric illness. [9] The first published report of the use of seizure
induction to treat mania using camphor was in 1785. [9]

Explore a medication that improved sleep time in clinical trials in patients with
insomnia Review trial data and more
Information from Industry
In 1934, the Hungarian neuropathologist Ladislas Joseph von Meduna began the
modern era of convulsive therapy by using intramuscular injection of camphor (soon
replaced with pentylenetetrazol) to treat catatonic schizophrenia. [9] In 1938, Italian
psychiatrist Lucio Bini and neurologist Ugo Cerletti performed the first electrical
induction of a series of seizures in a catatonic patient and produced a successful
treatment response. [9] One year later, ECT was introduced to the United States. [11]

Lack of adequate anesthesia or muscle relaxation during ECT led to fractures and
dislocations, and insufficient knowledge about the dose parameters of electrical
stimulation led to more severe cognitive adverse effects. [11] In 1940, curare was
developed for use as a muscle relaxant during ECT. [9] Until effective antipsychotic
drugs were developed in the 1950s, the only effective alternatives to ECT were
insulin shock therapy and lobotomy. [11]

In the 1950s, Max Fink was the first to apply rigorous scientific research methods to
ECT. [12] Succinylcholine, a depolarizing muscle relaxant, was introduced in 1951,
and the first controlled study of unilateral ECT was conducted in 1958. [9] In the
1960s, randomized clinical trials of the efficacy of ECT versus medications in the
treatment of depression showed response rates that were significantly higher with
ECT. [9]

In 1978, the American Psychiatric Association published the first Task Force Report
on ECT, with the goal of establishing standards for consent and the technical and
clinical aspects of the conduct of ECT. [9] In 1985, the National Institutes of Health
and National Institute of Mental Health Consensus Conference on ECT endorsed a
role for the use of ECT and advocated research and national standards of practice.
[9]

In 1988, randomized controlled clinical trials of ECT versus lithium showed that they
were equally effective in treating mania. [9] In 2000, Sarah Lisanby and colleagues
from Columbia University induced convulsive treatment with magnetic stimulation. [9]

Mechanism of action

The mechanism of action of ECT is not fully known. ECT affects multiple central
nervous system components, including hormones, neuropeptides, neurotrophic
factors, and neurotransmitters. [13]

The induction of a bilateral generalized seizure is required for both the beneficial
and adverse effects of ECT. [9] An increase in gamma­aminobutyric acid (GABA)
transmission and receptor antagonism has been observed, which raises the seizure
threshold during ECT. [14] ECT may also lead to an increase of endogenous opioids,
which may also have anticonvulsant properties. [12]

Positron emission tomography (PET) has been used to study the neurophysiological
effects of ECT. [9] In a literature review of studies assessing possible changes in
cerebral glucose metabolism by PET before and after ECT, reduction in glucose
metabolism after ECT in bilateral anterior and posterior frontal areas represented
the most consistent findings. [15]

Nearly every neurotransmitter system is affected by ECT, including beta­adrenergic,

serotonin, muscarinic, cholinergic, and dopaminergic systems. [9] Brain­derived
neurotrophic factor (BDNF), [16, 17] second­messenger systems, [9] and catechol­O­
methyltransferase (COMT) polymorphisms[18] may play a role in ECT.

Although many biomarkers have been studied, no ECT biomarker is routinely used
in clinical practice. [17]

Relevant Anatomy

In the central nervo/us system, the brain and spinal cord are the main centers where
correlation and integration of nervous information occur. Both the brain and spinal
cord are covered with a system of membranes, called meninges, and are suspended
in the cerebrospinal fluid; they are further protected by the bones of the skull and
the vertebral column.

The central nervous system is composed of large numbers of excitable nerve cells
and their processes, called neurons, which are supported by specialized tissue
called neuroglia. The long processes of a nerve cell are called axons or nerve fibers.
The interior of the central nervous system is organized into gray and white matter.
Gray matter consists of nerve cells embedded in neuroglia; it has a gray color.
White matter consists of nerve fibers embedded in neuroglia; it has a white color
due to the presence of lipid material in the myelin sheaths of many of the nerve
fibers. The billions of neurons in the brain are connected to neurons throughout the
body by trillions of synapses.

For more information about the relevant anatomy, see Central Nervous System
Anatomy and Brain Anatomy.

Indications

ECT is indicated for selected patients with major depressive disorder, bipolar
disorder, schizophrenia, and other disorders.

Major depressive disorder

ECT should be considered for patients in the acute phase of major depressive
disorder who have a high degree of symptom severity and functional impairment or
who have psychotic symptoms or catatonia. [19, 20] ECT may also be the treatment
of choice for patients in whom treatment response is urgently needed, such as
patients who are suicidal[19, 21] or those who are refusing food and are nutritionally
compromised. [19]

Bipolar disorder

ECT may be considered for patients with severe or treatment­resistant manic or

mixed episodes of bipolar disorder, [22, 23] or (in consultation with the psychiatrist) for
patients who prefer this treatment modality. [24] ECT also is a potential treatment for
those experiencing severe mania or depression during pregnancy. [24] ECT may be
efficacious in patients with rapid cycling bipolar disorder. [25] Mania resulting from
ECT is rare. [1]

In patients with life­threatening inanition (the exhausted condition that results from
lack of food and water), suicidality, [21] or psychosis, ECT is a reasonable alternative
treatment. [24] For patients who have depression with psychotic or catatonic features,
ECT should be considered. [24] Maintenance ECT may be considered for patients
whose acute episode of depression responded to ECT. [24]

Schizophrenia

ECT is effective for symptoms of acute schizophrenia but is not effective for chronic
schizophrenia. [9] In combination with antipsychotics, ECT may be considered for
patients with severe psychosis that has not responded to treatment with
antipsychotic medications. [26]

The greatest therapeutic benefit appears to occur when ECT is administered

concurrently with antipsychotic medications. [26, 27, 28] ECT also should be
considered for patients with prominent catatonic features that have not responded
to lorazepam. [26]

For patients with comorbid depression, ECT may be beneficial if depressive

symptoms are treatment­resistant or if features such as suicidal ideation and
behaviors or inanition are present. [26]

In the stable phase of schizophrenia, ECT may benefit some patients whose
condition has responded to ECT in the acute phase but for whom pharmacological
prophylaxis alone has been ineffective or cannot be tolerated. [26] ECT may be
especially effective when marked positive and affective symptoms are present. [29]

Other psychotic disorders

ECT is effective for psychotic disorders related to schizophrenia, such as

schizophreniform disorder and schizoaffective disorder. [1] In combination with
antipsychotics, ECT may be considered for patients with schizoaffective disorder
with severe psychosis that has not responded to treatment with antipsychotic
medications. [26]

Comorbid disorders

ECT is not recommended for the treatment of obsessive­compulsive disorder (OCD)

but may be considered for treating comorbid disorders such as major depressive
disorder, mania, and schizophrenia in patients with OCD. [30]

Other disorders and indications

ECT has been effective in the treatment of catatonia, [31] neuroleptic malignant
syndrome, [32] depression associated with Parkinson disease, [33, 34] pain, [35]
particular cases of delirium, [36] and acute confusion psychosis. [37] It has also been
effective in treating patients with intellectual disabilities who have treatment­
resistant mood or psychotic disorders. [38]

ECT may be useful in patients with major depressive disorder for whom medication
or psychotherapy has not been effective in maintaining stability during the
continuation phase. [19] ECT should be considered in patients whose condition has
failed to respond to medication trials, individuals who have not tolerated indicated
medications, or those who have previously shown a response to ECT. [9, 19] ECT
also should be considered in patients with melancholic[39] and atypical[40]
depression.

Contraindications

ECT has no absolute contraindications. Many medical conditions place patients at

an increased risk for complications and warrant closer monitoring, however. [9]

In a study of patients with major depressive disorder and comorbid borderline

personality disorder (BPD), patients with BPD did not experience the same degree
of improvement when treated with ECT as did patients with other personality
disorders or with no personality disorder. [41]

Preparation
Anesthesia

In the first several years of use, electroconvulsive therapy (ECT) was performed
without anesthesia. Since the late 1950s, however, ECT has been performed under
general anesthesia. [12] The goal is to produce a "light level" of anesthesia.
Excessive anesthesia may cause problems such as prolonged unconsciousness and
cardiovascular complications, and too little anesthesia may cause problems such as
incomplete unconsciousness and autonomic arousal. [1, 9]

Anesthetic medications used in ECT include the following[1] :

Methohexital (barbiturate)
Thiopental (barbiturate)
Etomidate (nonbarbiturate)
 Ketamine (nonbarbiturate)
Alfentanil (opioid)
Propofol (nonbarbiturate)

Methohexital is most commonly used[9] and is the preferred anesthetic for ECT
because of its established safety record, effectiveness, and low cost. [1] Inhalational
anesthesia with medications such as sevoflurane may also be an option. [42]

The cognitive outcome after ECT may be affected by the choice of the anesthetic
medication. [43] No matter which anesthetic medication is used, the appropriate dose
should be established at each treatment session, and adjustments should be made
at subsequent treatment sessions. [1]

Equipment

The ECT treatment and recovery areas should contain equipment to monitor vital
signs and provide initial management of medical emergencies. An optimal
treatment site includes separate functional areas for waiting, treatment, and
recovery. [1]

A stethoscope, a blood pressure measurement device, electrocardiographic and

pulse oximetry measurement devices, and an oxygen delivery system should be
present. Supplies for inducing anesthesia, providing ventilation, monitoring
physiologic functions (including seizure activity), and performing resuscitation should
be present.

Examples of ECT machines available in the United States include the Thymatron
System IV (Somatics, LLC, Lake Bluff, Ill) and the MECTA Spectrum 5000Q
(MECTA Corporation, Lake Oswego, Ore). Extensive details on equipment,
physiologic monitoring, and treatment site can be found in the American Psychiatric
Association's Task Force Report. [1]

Positioning

Common electrode positions in ECT include the bifrontotemporal, right unilateral,

and bifrontal positions. [44] Further research is needed for the asymmetric bilateral
position. [1, 45]

In the bifrontotemporal position[44] (commonly referred to as bilateral), electrodes

are placed bifrontotemporally, with the center of each electrode approximately 1
inch above the midpoint of an imaginary line drawn from the tragus to the external
canthus. [9]

In the right unilateral position, one electrode is typically placed over the
nondominant frontotemporal area, and the other electrode is placed on the
nondominant centroparietal scalp, just lateral to the midline vertex. [9] As the left
hemisphere is dominant in most people, unilateral electrode placement is almost
always over the right hemisphere. [9]

In the bifrontal position, the placement of an electrode on each side of the head is
more frontal than in standard bifrontotemporal placement.

In the asymmetric bilateral position, [45] the left electrode is moved about 6 cm
anterior from the standard frontotemporal position, and its lateral edge is medial to
the bony intersection ridge between the temple and the forehead. The right
electrode is in the standard frontotemporal position.

Anticholinergics

After the electrical stimulus is administered during ECT, a short period of

bradycardia occurs, which then converts to tachycardia during the seizure. Prior to
anesthesia, administration of anticholinergics (eg, atropine, glycopyrrolate) can
reduce the risk of vagally mediated bradyarrhythmias or asystole[1] and minimize
oral and respiratory secretions. [9]

Anticholinergics may be especially useful for patients taking beta­adrenergic

receptor blockers. [1, 9] Due to lack of an evidence base in moderating the
cardiovascular effects of ECT, however, not all clinicians routinely use
anticholinergics. [1]

Anticholinergics can increase preexisting tachycardia and can cause constipation,

fecal impaction, and urinary retention. [1]

Neuromuscular Blocking

Neuromuscular blockers are administered to prevent bone fractures and physical

injury related to motor activity during the seizure that occurs with electroconvulsive
therapy. [9, 11, 12] This is especially important if the patient has osteoporosis or a
history of spinal injury; [11, 12] in these cases, complete relaxation may be indicated.
[1]

Anesthesia support is needed for administration of neuromuscular blocking agents.

The preferred neuromuscular blocker is succinylcholine, a depolarizing drug. [1]
Atracurium, mivacurium, rocuronium, and rapacuronium are alternatives to
succinylcholine. [1]
A nondepolarizing muscle relaxant may be indicated in patients with
pseudocholinesterase deficiency, hypercalcemia, severe neuromuscular disease,
severe osteoporosis, or a personal or family history of malignant hyperthermia. [1]

Prior to electrical stimulation, the sufficiency of muscle relaxation is determined by

the reduction or loss of knee, ankle, or plantar withdrawal reflexes; loss of muscle
tone; the reduction or failure to respond to a nerve stimulator; or any combination of
these factors. [1]

Pretreatment Evaluation

No routine pretreatment evaluation for patients undergoing ECT is established. A

collaborative approach between the ECT psychiatrist, medical consultants, and
anesthesia provider is a more meaningful and inclusive method than simply asking
for clearance. [46]

A pre­ECT evaluation should include the following components[1, 9, 11, 12, 44, 47, 46] :

A thorough psychiatric history and examination, including history of response

to ECT and other treatments
A medical history and examination, with special attention to cardiovascular,
pulmonary, neurological, and musculoskeletal systems
A history of dental problems and examination for loose or missing teeth
A history of personal and family experiences with anesthesia
A cognitive assessment (at minimum, evaluation of orientation and memory)

Though no routine set of laboratory tests for patients before undergoing ECT has
been established, commonly ordered tests prior to initiation of ECT include the
following:

Complete blood count

Serum chemistry
Renal function
Electrocardiogram
Urinalysis
Chest radiograph (especially with cardiovascular or pulmonary disease or
history of smoking)
Electroencephalogram (guided by history and examination)
Neuroradiological/neuropsychological tests (guided by history and
examination)
Spinal radiograph (especially with known or suspected spinal disease)
Consultation with medical specialties such as cardiology, neurology,
neurosurgery, or endocrinology as required by special medical conditions

Informed Consent

Informed consent is an important part of the process for ECT. In a descriptive

systematic review of papers and reports that included 134 testimonies,
approximately half the patients reported that they had received sufficient
information about ECT and adverse effects. In that review, approximately one third
of patients did not feel they had freely consented to ECT, even when they had
signed a consent form. [48]

No patient with a capacity to give voluntary consent should be treated with ECT
without his or her written, informed consent. No clear consensus about how to
determine capacity to consent has been established. The capacity to consent has
generally been interpreted as evidence that the patient can understand information
about the procedure and can act responsibly on the basis of this information. [1, 47]

The use of involuntary ECT is rare. Involuntary ECT should be reserved for patients
who need emergency treatment and who have a legally appointed guardian who has
agreed to the use of ECT. [9] Clinicians must be familiar with local, state, [49] and
federal laws about the use of ECT. [9]

The informed­consent process should be documented in the patient's medical record

and should include a discussion of the disorder, its natural course, and the option of
receiving no treatment. [9] Printed literature and videotapes about ECT may be
useful. [9] The family of the patient should be included in the discussion. [50]

The consent form for ECT should include the following information[1, 47] :

Who is recommending ECT and why

A description of treatment alternatives
A detailed description of how, when, and where ECT will be carried out
A discussion of options regarding electrode placement
The typical range for the number of treatments
A statement that the treatment is not guaranteed to be successful
A statement concerning the need for continuation or maintenance treatment
Discussion of the possible risks, including death, cardiac dysfunction,
confusion, and memory impairment
A statement that the consent also applies to emergency treatment that may
be clinically necessary during periods when the patient is unconscious
A listing of patient requirements during the ECT course, such as taking
nothing by mouth after midnight
A statement that the patient has had an opportunity to ask questions and
indication of who can be contacted with further questions
 A statement that consent is voluntary and can be withdrawn at any time

Electroconvulsive Therapy with Comorbidity

Concurrent medical conditions and their treatments may affect the response to and
risks associated with electroconvulsive therapy. [1]

Neurological comorbidities

Caution is advised for patients with space­occupying intracranial lesions, as these

individuals are at increased risk for edema and brain herniation after ECT. [9]
Patients with intracerebral lesions that lack a mass effect can safely undergo ECT.
[12]

ECT increases intracranial pressure and blood flow to the brain. [12] Patients who
have increased intracerebral pressure or are at risk for cerebral bleeding, such as
those with cerebrovascular disease and aneurysms, are at increased risk during
ECT. [9] Patients with very recent strokes are of special concern. [1]

ECT has been safely used after coil embolization of a cerebral aneurysm. [51] ECT
has been used in the presence of Charcot­Marie­Tooth disease, [52] arachnoid cysts,
[53, 54] epilepsy, [1, 55] myasthenia gravis, [1] and multiple sclerosis. [1]

Cardiac comorbidities

Patients with cardiac disease should be evaluated by a cardiologist who can assist
with the patient’s management during the course of ECT. [1, 12, 56] In patients with
unstable angina, uncompensated congestive heart failure, uncontrolled
hypertension, high­grade atrioventricular block, and symptomatic ventricular
arrhythmias, ECT raises the risk of symptoms from these cardiac conditions. [1]
Patients with hypertension should be stabilized with antihypertensive medications
before undergoing ECT. [9]

Patients with a recent myocardial infarction (MI) are at high risk of cardiac
complications such as MI, although the risk is greatly decreased 2 weeks after the
MI and is further reduced 3 months after the MI. [9]

With a proper pre­ECT cardiac and pacemaker/defibrillator assessment, patients

with cardiac pacemakers and implantable cardioverter defibrillators can safely
undergo ECT. [57] ECT has been used in the presence of severe aortic stenosis[58] ,
and it has been used after heart transplantation, though further studies are needed.
[59]

Other comorbidities

Patients who have medical disorders associated with autonomic sensitivity (eg,
clinically evident hyperthyroidism, pheochromocytoma), with sensitivity to anesthesia
(eg, amyotrophic lateral sclerosis, porphyria, pseudocholinesterase deficiency), or
with cognitive sensitivity (eg, traumatic brain injury) may require more extensive
workup and closer monitoring during ECT. [11]

Patients with gastroesophageal reflux disease may experience worsening symptoms

during ECT, due to stimulation of the vagus nerve. [12]

Patients with diabetes, metabolic disorders (eg, hyperkalemia, hypokalemia,

hyponatremia), chronic obstructive pulmonary disease, hypercoagulable states,
glaucoma, and renal disease require close monitoring during ECT. [1, 60]

Electroconvulsive Therapy and Medications

Some medications may be continued during ECT, some medications are decreased
or withdrawn, and some augment ECT. [1]

Medications such as antihypertensives, antianginals, antiarrhythmics (except

lidocaine), bronchodilators (except theophylline), glaucoma medications (except
long­acting cholinesterase inhibitors), and corticosteroids[1] may be safely given prior
to ECT. Antacid medications and proton pump inhibitors may be safely used. [12]

Diuretics and hypoglycemics may be withheld until after an ECT treatment. [1, 11]
Theophylline should be discontinued if possible. [1, 11]

Anticonvulsants should be lowered in dose as much as clinically possible during

ECT, because antiepileptics may raise seizure threshold, adversely affect seizure
expression, or possibly affect clinical efficacy. [1] One review found that the
combination of various anticonvulsants and ECT was safe and effective, though no
evidence indicated that this combination increased efficacy. [61]

Monoamine oxidase inhibitors (MAOIs) are generally safe. Nevertheless, some

clinicians withdraw MAOIs 7­14 days before ECT. [1]

The combination of ECT and antipsychotics may be more effective in schizophrenia

than either treatment alone. [1] Although definitive conclusions cannot be made, the
combination of ECT and antipsychotics is safe and effective in schizophrenia,
especially in patients whose symptoms are refractory to conventional treatments. [62,
63]
Debate about the safety of lithium during ECT is ongoing, as some patients have
no problems but others may have a higher risk for delirium or prolonged seizures. [1,
12, 44, 64] Benzodiazepines should be lowered in dose or discontinued if possible. [1,
12]

Most antidepressants can be safely combined with ECT. [46] Caution is

recommended with high doses of bupropion. [1]

Electroconvulsive Therapy and Pediatrics

The use of ECT in the pediatric population is controversial. [65] The American
Academy of Child and Adolescent Psychiatry published a practice parameter for the
use of ECT with adolescents in December 2004.

Diagnostic considerations for ECT in an adolescent patient [66] include severe or

persistent major depression or mania[67] with or without psychotic features,
schizoaffective disorder, schizophrenia, catatonia, [68] or neuroleptic malignant
syndrome. The symptoms must be severe, persistent, and significantly disabling,
and they may include life­threatening symptoms.

Before considering ECT in children and adolescents, lack of treatment response

should be documented. Lack of treatment response is defined as failure to respond
to at least 2 adequate trials of appropriate psychopharmacological agents
accompanied by other appropriate treatment modalities. [66] Every child or
adolescent patient being considered for ECT should receive an independent
evaluation from a psychiatrist who is not directly responsible for the patient's
treatment and who is knowledgeable about ECT. [66]

The response rate for mood disorders to ECT in the pediatric population is 75­
100%. The response rate for psychotic disorders is 50­60%. [66]

Electroconvulsive Therapy in the Elderly

A high proportion of patients who receive ECT are in the geriatric age group. [1] In
elderly patients, ECT has been used to treat catatonia, [69] bipolar mania, [70] and
psychotic disorders. [69]

Generally, geriatric patients with depression have better outcomes with ECT than
do younger patients. [1] ECT is especially indicated for patients with depression who
are at risk for harm because of psychosis, suicidal ideation, or severe malnutrition,
[71, 72, 73] but it is also helpful for treatment­resistant nonpsychotic major

depression. [74]

Seizure threshold may rise with increasing age, and effective seizures may be hard
to induce. [1] Geriatric patients may be at a higher risk for persistent confusion and
greater memory deficits during and after ECT. [1]

A 2003 Cochrane Database review of ECT for elderly patients with depression
found that solid conclusions could not be drawn as to whether ECT was more
effective than antidepressants or regarding the safety and adverse effects of ECT in
these patients. [75]

Electroconvulsive Therapy in Pregnancy

ECT is considered safe and effective for the mother and fetus in the treatment of
major depressive disorder during pregnancy. [19] ECT is a potential treatment for
patients with bipolar disorder who are experiencing mixed episodes[23] , severe
mania, or severe depression during pregnancy. [24]

ECT should be considered for women who prefer to avoid extended exposure to
psychotropic medication during pregnancy[76] or for those pregnant women whose
symptoms fail to respond to standard therapy. [76, 77] Obstetric consultation should
be obtained and fetal monitoring should be used, when appropriate.

Patients in late pregnancy should lie on their left side during ECT to ensure
adequate blood flow to the fetus. Hyperventilation is to be avoided. [78]

Transmission of anesthesia medications across the maternal­fetal barrier is

considered to be minimal. [12] ECT is considered relatively safe in terms of
teratogenicity and neonatal toxicity. [1] Because of an increased risk of gastric reflux
and possible aspiration, pregnant women may be premedicated with a
nonparticulate antacid, such as sodium citrate. [1]

Generally, breastfeeding does not need to be interrupted during ECT. Anesthetic

agents pose little risk to the nursing infant. Exposure of nursing infants to
medications may be decreased if the mother delays feeding for several hours after
an ECT treatment. Alternatively, breast milk may be collected and stored before an
ECT treatment and given via bottle after an ECT treatment. [1]

Technique
Overview
The electrical stimulus must be sufficient to induce a seizure. A brief pulse
waveform is used in modern electroconvulsive therapy (ECT) machines. [9] The dose
is measured in millicoulombs of charge delivered. [44]

Three methods are used to determine stimulus intensity and dosing, as follows[1, 44]
:

Empirical titration
Formula­based titration
Fixed dosages

In empirical titration, progressively higher doses are given during the first ECT
session until seizure threshold is reached. This provides the most precise method
for determining seizure threshold. [1] In formula­based titration, the dose is based on
factors such as age, gender, and electrode placement. In the third method, a fixed
dose is given independent of patient or other factors.

A fourth method, called the glissando technique, in which the stimulus intensity is
progressively increased during delivery from a subconvulsive to a convulsive level,
has not been justified. It is now of only historical interest. [1]

When determining stimulus intensity and dosing, changes in seizure threshold

during the course of treatment should also be considered. A patient's seizure
threshold may increase anywhere from 25­200%. [1]

Seizure Quality

Seizure duration has little bearing on efficacy of electroconvulsive therapy, and

seizure duration has a complex association with stimulus intensity. Nevertheless, if
the seizure duration is less than 15 seconds in motor and EEG manifestations, the
seizure was very likely limited by insufficient electrical stimulation. [1]

The EEG is used to confirm seizure activity and to document seizure duration. [44]
Seizure motor activity is monitored using the "cuff" procedure, in which distribution
of a muscle relaxant is blocked to the hand or foot via a tourniquet to maintain the
potential for muscle contraction. [1, 44]

Frequency of Treatments

In the United States, ECT is most commonly performed 3 times per week
regardless of electrode placement. [1] More frequent regimens are not justified. [1]
Treatments 2 times per week may result in less memory impairment than
treatments 3 times per week. [1, 9] Compared with treatments administered 3 times
per week, twice­weekly treatments result in the same degree of final clinical
improvement, although possibly at a slower rate of response. [1]

Multiple monitored ECT (MMECT) involves treatment in which more than one
adequate seizure is induced in the same session under continuous anesthesia. [1, 9]
Urgent clinical scenarios such as neuroleptic malignant syndrome may warrant
MMECT, but routine use is not recommended. [1, 9]

Number of Treatments

The number of treatments needed to achieve a full clinical response in patients

varies widely. Although the typical number of treatments is 6­12, [12, 44] some
patients may respond after a few treatments, and some patients may not respond
until after 10 treatments. [1] The total number should be a function of the patient's
degree and rate of clinical improvement, as well as the severity of cognitive adverse
effects. [1] Treatment is stopped when maximal improvement is reached. [1, 11]

Post­Procedure
Complications

The principal complications of electroconvulsive therapy (ECT) are mortality and

cognitive adverse effects.

Mortality

Cardiovascular complications (eg, arrhythmias[79] ) and pulmonary complications are

the leading causes of mortality due to ECT. [1] } The mortality rate for ECT is
estimated to be 1 per 10,000 patients or 1 per 80,000 treatments. This is about the
same as that associated with minor surgery. [1] The mortality rate may be higher in
patients with severe medical disorders, though it may be lower than that with
tricyclic antidepressant therapy. [1]

Cognitive adverse effects

Cognitive adverse effects are the major limitations to the use of ECT. [1] The most
severe effects are observed postictally, with a brief period of disorientation and
impairments in attention, praxis, and memory. [1] The effects reverse over time. [1]
Individual patients vary significantly in the extent and severity of cognitive adverse
effects experienced after ECT. [1] Various biochemical, electrophysiological, and
neuroimaging correlates of the cognitive adverse effects of ECT exist. [80]

The particular ECT technique used has a significant impact on cognitive deficits,
and modifications may need to be made, [81] such as switching to unilateral ECT,
lowering the stimulus dose, increasing the time interval between treatments, or
stopping medications that may increase cognitive adverse effects. [1]

Anterograde and retrograde amnesia may result from ECT. [1] After ECT,
anterograde amnesia resolves rapidly. With retrograde amnesia, deficits are
greatest for events closest to the time of treatment. [1] Postictal delirium may occur
in a minority of patients. [1]

A prospective, naturalistic, longitudinal study of clinical and cognitive outcomes in

patients with major depression treated at 7 facilities found that cognitive outcomes
varied across facilities and that differences in ECT technique largely accounted for
these differences. [82] A recent review in older adults found mixed results regarding
the impact of ECT on cognitive domains, aside from interictal slowing of information
processing speed. [83]

Other adverse effects

Asystole has been reported in patients who undergo ECT. [84, 85] Prolonged seizures
and status epilepticus may be more likely when patients receive medications that
lower seizure threshold. [1] Prolonged apnea is rare but may occur in patients who
metabolize succinylcholine slowly. [1]

Headache is common. It can be treated with medications such as aspirin,

acetaminophen, nonsteroidal anti­inflammatory drugs, sumatriptan, [86] and, rarely,
more potent analgesics such as codeine. [1] Muscle soreness and nausea may occur.
[1] Mania resulting from ECT is rare. [1]

Continuation Electroconvulsive Therapy

Continuation ECT is used for prevention of relapse. [46] Because of the high risk of
relapse after ECT, especially during the first few months, the argument for
aggressive continuation therapy is compelling. [1]

Indications for continuation ECT include a history of ECT­responsive illness, patient

preference, resistance or intolerance to medications alone, and ability of the patient
(or surrogate consenter) to provide informed consent and adhere to the treatment
plan. [1]

In a small study of patients with schizophrenia or schizophreniform disorder,

continuation ECT plus neuroleptics was effective and safe for relapse prevention,
even in patients with medication­resistant schizophrenia who relapsed after
responding to acute ECT. [87]

A comparison multisite randomized parallel design study of continuation ECT and

the combination of lithium and nortriptyline for relapse prevention in major
depression found that both these modes of therapy had limited efficacy but were
superior to placebo. [88] In a randomized controlled trial of continuation
pharmacotherapy in patients with depression after response to ECT, a lower relapse
rate was found with nortriptyline plus lithium (39%) than with nortriptyline alone
(60%) or placebo (84%). [89]

Maintenance Electroconvulsive Therapy

Maintenance ECT is for prevention of recurrence. [46] Indications are the same as
those for continuation ECT. [1] In a longitudinal, randomized, single­blind study of
elderly patients with unipolar psychotic depression who remitted to ECT plus
nortriptyline, the mean survival time was significantly longer in the
continuation/maintenance ECT plus nortriptyline subgroup than in the nortriptyline
subgroup. [90]

Pharmacological Therapy

Pharmacological therapy after ECT varies with a patient's diagnosis. [1] Patients with
major depressive disorder and whose symptoms are resistant to pharmacological
therapy may benefit prophylactically from the same class of medication during
maintenance therapy after ECT. [91]

Regarding clinical predictors, lower remission rates after acute ECT may be
associated with medication resistance and chronicity in patients with major
depression but are not associated with age or burden of physical illness. [92]
Melancholic features may not predict response to ECT. [93] In patients with
nonpsychotic major depression, antidepressant medication failure may not predict
acute remission with ECT. [94]

Psychotherapy

Individual, family, or group psychotherapy is helpful for some patients after ECT to
treat residual symptoms, cope with stress, and encourage a return to normal life. [1]
Preliminary evidence suggests that cognitive­behavioral therapy may lengthen the
antidepressant effects of ECT. [95]

Contributor Information and Disclosures

Author
Raj K Kalapatapu, MD Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons

Raj K Kalapatapu, MD is a member of the following medical societies: American Academy of Addiction
Psychiatry, American Academy of Child and Adolescent Psychiatry, American Association for Geriatric
Psychiatry, American Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Editor­in­Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor
Dennis M Popeo, MD Assistant Professor of Psychiatry, Icahn School of Medicine at Mount Sinai; Director,
Medical Student Education, Director, Geriatric Psychiatry Clinic, Mount Sinai Medical Center

Dennis M Popeo, MD is a member of the following medical societies: American Medical Association, American
Psychiatric Association, Gay and Lesbian Medical Association, Medical Society of the State of New York

Disclosure: Nothing to disclose.

Additional Contributors
Andrew K Chang, MD Associate Professor, Department of Emergency Medicine, Albert Einstein College of
Medicine, Montefiore Medical Center

Andrew K Chang, MD is a member of the following medical societies: American Academy of Emergency
Medicine, American Academy of Neurology, American College of Emergency Physicians, Society for Academic
Emergency Medicine

Disclosure: Nothing to disclose.

References

1. American Psychiatric Association. The Practice of Electroconvulsive Therapy: Recommendations for

Treatment, Training, and Privileging. A Task Force Report of the American Psychiatric Association. 2nd ed.
American Psychiatric Publishing; 2001.

2. Ross CA. The sham ECT literature: implications for consent to ECT. Ethical Hum Psychol Psychiatry. 2006
Spring. 8(1):17­28. [Medline].

3. Lauber C, Nordt C, Falcato L, Rossler W. Can a seizure help? The public's attitude toward
electroconvulsive therapy. Psychiatry Res. 2005 Apr 15. 134(2):205­9. [Medline].

4. Arshad M, Arham AZ, Arif M, et al. Awareness and perceptions of electroconvulsive therapy among
psychiatric patients: a cross­sectional survey from teaching hospitals in Karachi, Pakistan. BMC Psychiatry.
2007 Jun 21. 7:27. [Medline]. [Full Text].

5. Lauber C, Nordt C, Rossler W. Recommendations of mental health professionals and the general
population on how to treat mental disorders. Soc Psychiatry Psychiatr Epidemiol. 2005 Oct. 40(10):835­43.
[Medline].

6. Burstow B. Electroshock as a form of violence against women. Violence Against Women. 2006 Apr.
12(4):372­92. [Medline].

7. McDonald A, Walter G. The portrayal of ECT in American movies. J ECT. 2001 Dec. 17(4):264­74.
[Medline].

8. American Psychiatric Association. Electroconvulsive Therapy (ECT) Position Statement. December 2007.
Accessed February 4, 2009. [Full Text].

9. Sadock BJ, Sadock VA. Brain Stimulation Methods. Kaplan & Sadock's Synopsis of Psychiatry: Behavioral
Sciences/Clinical Psychiatry. 10th ed. Lippincott Williams & Wilkins; 2007. Chapter 36.37.

10. Ottosson JO, Fink M. Ethics in Electroconvulsive Therapy. New York: Routledge; 2004.

11. Pandya M, Pozuelo L, Malone D. Electroconvulsive therapy: what the internist needs to know. Cleve Clin J
Med. 2007 Sep. 74(9):679­85. [Medline].

12. Taylor S. Electroconvulsive therapy: a review of history, patient selection, technique, and medication
management. South Med J. 2007 May. 100(5):494­8. [Medline].

13. Wahlund B, von Rosen D. ECT of major depressed patients in relation to biological and clinical variables: a
brief overview. Neuropsychopharmacology. 2003 Jul. 28 Suppl 1:S21­6. [Medline].

14. Palmio J, Huuhka M, Saransaari P, et al. Changes in plasma amino acids after electroconvulsive therapy of
depressed patients. Psychiatry Res. 2005 Dec 15. 137(3):183­90. [Medline].

15. Schmidt EZ, Reininghaus B, Enzinger C, Ebner C, Hofmann P, Kapfhammer HP. Changes in brain
metabolism after ECT­positron emission tomography in the assessment of changes in glucose metabolism
subsequent to electroconvulsive therapy­­lessons, limitations and future applications. J Affect Disord. 2008
Feb. 106(1­2):203­8. [Medline].
16. Bocchio­Chiavetto L, Zanardini R, Bortolomasi M, et al. Electroconvulsive Therapy (ECT) increases serum
Brain Derived Neurotrophic Factor (BDNF) in drug resistant depressed patients. Eur
Neuropsychopharmacol. 2006 Dec. 16(8):620­4. [Medline].

17. Marano CM, Phatak P, Vemulapalli UR, et al. Increased plasma concentration of brain­derived neurotrophic
factor with electroconvulsive therapy: a pilot study in patients with major depression. J Clin Psychiatry.
2007 Apr. 68(4):512­7. [Medline].

18. Anttila S, Huuhka K, Huuhka M, et al. Catechol­O­methyltransferase (COMT) polymorphisms predict

treatment response in electroconvulsive therapy. Pharmacogenomics J. 2008 Apr. 8(2):113­6. [Medline].

19. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Major Depressive
Disorder, Second Edition. American Psychiatric Association Practice Guidelines. [Full Text].

20. American Psychiatric Association. Guideline Watch: Practice Guideline for the Treatment of Patients with
Major Depressive Disorder, Second Edition. American Psychiatric Association Practice Guidelines. [Full
Text].

21. American Psychiatric Association. Practice Guideline for the Assessment and Treatment of Patients With
Suicidal Behaviors. American Psychiatric Association Practice Guidelines. [Full Text].

22. Gitlin M. Treatment­resistant bipolar disorder. Mol Psychiatry. 2006 Mar. 11(3):227­40. [Medline].

23. Valenti M, Benabarre A, Garcia­Amador M, Molina O, Bernardo M, Vieta E. Electroconvulsive therapy in

the treatment of mixed states in bipolar disorder. Eur Psychiatry. 2008 Jan. 23(1):53­6. [Medline].

24. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Bipolar Disorder,
Second Edition. American Psychiatric Association Practice Guidelines. [Full Text].

25. Papadimitriou GN, Dikeos DG, Soldatos CR, Calabrese JR. Non­pharmacological treatments in the
management of rapid cycling bipolar disorder. J Affect Disord. 2007 Feb. 98(1­2):1­10. [Medline].

26. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Schizophrenia,
Second Edition. American Psychiatric Association Practice Guidelines. [Full Text].

27. Painuly N, Chakrabarti S. Combined use of electroconvulsive therapy and antipsychotics in schizophrenia:
the Indian evidence. A review and a meta­analysis. J ECT. 2006 Mar. 22(1):59­66. [Medline].

28. Tharyan P, Adams CE. Electroconvulsive therapy for schizophrenia. Cochrane Database Syst Rev. 2005
Apr 18. CD000076. [Medline].

29. Chanpattana W, Andrade C. ECT for treatment­resistant schizophrenia: a response from the far East to
the UK. NICE report. J ECT. 2006 Mar. 22(1):4­12. [Medline].

30. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Obsessive­
Compulsive Disorder. American Psychiatric Association Practice Guidelines. [Full Text].

31. Weder ND, Muralee S, Penland H, Tampi RR. Catatonia: a review. Ann Clin Psychiatry. 2008 Apr­Jun.
20(2):97­107. [Medline].

32. Strawn JR, Keck PE Jr, Caroff SN. Neuroleptic malignant syndrome. Am J Psychiatry. 2007 Jun.
164(6):870­6. [Medline].

33. Veazey C, Aki SO, Cook KF, Lai EC, Kunik ME. Prevalence and treatment of depression in Parkinson's
disease. J Neuropsychiatry Clin Neurosci. 2005 Summer. 17(3):310­23. [Medline].

34. Balke LD, Varma A. A case of long­term maintenance ECT in a 78­year­old with depression and possible
Parkinson's disease. CNS Spectr. 2007 May. 12(5):325­6. [Medline].

35. Mowla A, Ashkani H, Firozabadi A, et al. Relief of acute intractable traumatic pain with ECT. J Psychiatr
Pract. 2007 Jan. 13(1):55­7. [Medline].

36. American Psychiatric Association. Practice Guideline for the Treatment of Patients With Delirium.
American Psychiatric Association Practice Guidelines. [Full Text].

37. Neuhaus AH, Katchanov J, Opgen­Rhein C, Neu P, Jockers­Scherubl MC. Electroconvulsive monotherapy
in the treatment of acute confusion psychosis. A case report. Pharmacopsychiatry. 2005 Nov. 38(6):330­2.
[Medline].

38. Reinblatt SP, Rifkin A, Freeman J. The efficacy of ECT in adults with mental retardation experiencing
psychiatric disorders. J ECT. 2004 Dec. 20(4):208­12. [Medline].

39. Brown WA. Treatment response in melancholia. Acta Psychiatr Scand Suppl. 2007. 125­9. [Medline].

40. Husain MM, McClintock SM, Rush AJ, et al. The efficacy of acute electroconvulsive therapy in atypical
depression. J Clin Psychiatry. 2008 Mar. 69(3):406­11. [Medline].

41. Feske U, Mulsant BH, Pilkonis PA, et al. Clinical outcome of ECT in patients with major depression and
comorbid borderline personality disorder. Am J Psychiatry. 2004 Nov. 161(11):2073­80. [Medline].

42. Rasmussen KG, Laurila DR, Brady BM, et al. Anesthesia outcomes in a randomized double­blind trial of
sevoflurane and thiopental for induction of general anesthesia in electroconvulsive therapy. J ECT. 2007
Dec. 23(4):236­8. [Medline].

43. MacPherson RD, Loo CK. Cognitive impairment following electroconvulsive therapy­­does the choice of
anesthetic agent make a difference?. J ECT. 2008 Mar. 24(1):52­6. [Medline].

44. Lisanby SH. Electroconvulsive therapy for depression. N Engl J Med. 2007 Nov 8. 357(19):1939­45.
[Medline].

45. Swartz CM. Asymmetric bilateral right frontotemporal left frontal stimulus electrode placement for
electroconvulsive therapy. Neuropsychobiology. 1994. 29(4):174­8. [Medline].
46. Greenberg RM, Kellner CH. Electroconvulsive therapy: a selected review. Am J Geriatr Psychiatry. 2005
Apr. 13(4):268­81. [Medline].

47. Electroconvulsive Therapy. Blazer DG, Steffens DC, Busse EW. Textbook of Geriatric Psychiatry. 3rd ed.
Washington, DC: American Psychiatric Publishing; 2004. Chapter 25; 413­426.

48. Rose DS, Wykes TH, Bindman JP, Fleischmann PS. Information, consent and perceived coercion: patients'
perspectives on electroconvulsive therapy. Br J Psychiatry. 2005 Jan. 186:54­9. [Medline].

49. Harris V. Electroconvulsive therapy: administrative codes, legislation, and professional recommendations. J
Am Acad Psychiatry Law. 2006. 34(3):406­11. [Medline].

50. McCall WV. Electroconvulsive therapy: all in the family. J ECT. 2007 Dec. 23(4):213­4. [Medline].

51. Okamura T, Kudo K, Sata N, Sameshima T, Doi N, Kato N. Electroconvulsive therapy after coil
embolization of cerebral aneurysm: a case report and literature review. J ECT. 2006 Jun. 22(2):148­9.
[Medline].

52. Laenger A, Leicht G, Schule C, Baghai TC, Lindhaus S, Rupprecht R. Electroconvulsive therapy in a
patient with concomitant depression and charcot­marie­tooth disease. Am J Psychiatry. 2008 Jun.
165(6):776­7. [Medline].

53. Hanretta AT, Akra I, Malek­Ahmadi P. Electroconvulsive therapy and arachnoid cysts. J ECT. 2007 Jun.
23(2):126­7. [Medline].

54. Perry CL, Lindell EP, Rasmussen KG. ECT in patients with arachnoid cysts. J ECT. 2007 Mar. 23(1):36­7.
[Medline].

55. Seethalakshmi R, Krishnamoorthy ES. Depression in epilepsy: phenomenology, diagnosis and

management. Epileptic Disord. 2007 Mar. 9(1):1­10. [Medline].

56. Solimene MC. Electroconvulsive therapy and the heart. Int J Cardiol. 2007 Jan 2. 114(1):103. [Medline].

57. Dolenc TJ, Barnes RD, Hayes DL, Rasmussen KG. Electroconvulsive therapy in patients with cardiac
pacemakers and implantable cardioverter defibrillators. Pacing Clin Electrophysiol. 2004 Sep. 27(9):1257­
63. [Medline].

58. O'Reardon JP, Cristancho MA, Cristancho P, Fontecha JF, Weiss D. Electroconvulsive therapy in a 96­year­
old patient with severe aortic stenosis: a case report and review of the literature. J ECT. 2008 Mar.
24(1):96­8. [Medline].

59. Fusar­Poli P, Picchioni M, Martinelli V, et al. Anti­depressive therapies after heart transplantation. J Heart
Lung Transplant. 2006 Jul. 25(7):785­93. [Medline].

60. Cohen SD, Norris L, Acquaviva K, Peterson RA, Kimmel PL. Screening, diagnosis, and treatment of
depression in patients with end­stage renal disease. Clin J Am Soc Nephrol. 2007 Nov. 2(6):1332­42.
[Medline].

61. Sienaert P, Peuskens J. Anticonvulsants during electroconvulsive therapy: review and recommendations. J
ECT. 2007 Jun. 23(2):120­3. [Medline].

62. Havaki­Kontaxaki BJ, Ferentinos PP, Kontaxakis VP, Paplos KG, Soldatos CR. Concurrent administration
of clozapine and electroconvulsive therapy in clozapine­resistant schizophrenia. Clin Neuropharmacol. 2006
Jan­Feb. 29(1):52­6. [Medline].

63. Braga RJ, Petrides G. The combined use of electroconvulsive therapy and antipsychotics in patients with
schizophrenia. J ECT. 2005 Jun. 21(2):75­83. [Medline].

64. Dolenc TJ, Rasmussen KG. The safety of electroconvulsive therapy and lithium in combination: a case
series and review of the literature. J ECT. 2005 Sep. 21(3):165­70. [Medline].

65. Stein D, Weizman A, Bloch Y. Electroconvulsive therapy and transcranial magnetic stimulation: can they
be considered valid modalities in the treatment of pediatric mood disorders?. Child Adolesc Psychiatr Clin
N Am. 2006 Oct. 15(4):1035­56, xi. [Medline].

66. American Academy of Child and Adolescent Psychiatry. Practice Parameter for Use of Electroconvulsive
Therapy With Adolescents. American Academy of Child and Adolescent Psychiatry Practice Parameters.
[Full Text].

67. Kowatch RA, Fristad M, Birmaher B, Wagner KD, Findling RL, Hellander M. Treatment guidelines for
children and adolescents with bipolar disorder. J Am Acad Child Adolesc Psychiatry. 2005 Mar. 44(3):213­
35. [Medline].

68. Zaw FK. ECT and the youth: catatonia in context. Int Rev Neurobiol. 2006. 72:207­31. [Medline].

69. Wilkins KM, Ostroff R, Tampi RR. Efficacy of electroconvulsive therapy in the treatment of nondepressed
psychiatric illness in elderly patients: a review of the literature. J Geriatr Psychiatry Neurol. 2008 Mar.
21(1):3­11. [Medline].

70. Aziz R, Lorberg B, Tampi RR. Treatments for late­life bipolar disorder. Am J Geriatr Pharmacother. 2006
Dec. 4(4):347­64. [Medline].

71. Dombrovski AY, Mulsant BH. The evidence for electroconvulsive therapy (ECT) in the treatment of severe
late­life depression. ECT: the preferred treatment for severe depression in late life. Int Psychogeriatr. 2007
Feb. 19(1):10­4, 27­35; discussion 24­6. [Medline]. [Full Text].

72. Beyer JL. Managing depression in geriatric populations. Ann Clin Psychiatry. 2007 Oct­Dec. 19(4):221­38.
[Medline].

73. Unutzer J. Clinical practice. Late­life depression. N Engl J Med. 2007 Nov 29. 357(22):2269­76. [Medline].

74. Driscoll HC, Karp JF, Dew MA, Reynolds CF 3rd. Getting better, getting well: understanding and managing
 partial and non­response to pharmacological treatment of non­psychotic major depression in old age. Drugs
Aging. 2007. 24(10):801­14. [Medline].

75. Van der Wurff FB, Stek ML, Hoogendijk WL, Beekman AT. Electroconvulsive therapy for the depressed
elderly. Cochrane Database Syst Rev. 2003. CD003593. [Medline]. [Full Text].

76. Cohen LS, Nonacs R, Viguera AC, Reminick A. Diagnosis and treatment of depression during pregnancy.
CNS Spectr. 2004 Mar. 9(3):209­16. [Medline].

77. Richards DS. Is electroconvulsive therapy in pregnancy safe?. Obstet Gynecol. 2007 Aug. 110(2 Pt 2):451­
2. [Medline].

78. Eberhard­Gran M, Eskild A, Opjordsmoen S. Treating mood disorders during pregnancy: safety
considerations. Drug Saf. 2005. 28(8):695­706. [Medline].

79. Nuttall GA, Bowersox MR, Douglass SB, et al. Morbidity and mortality in the use of electroconvulsive
therapy. J ECT. 2004 Dec. 20(4):237­41. [Medline].

80. Nobler MS, Sackeim HA. Neurobiological correlates of the cognitive side effects of electroconvulsive
therapy. J ECT. 2008 Mar. 24(1):40­5. [Medline].

81. Prudic J. Strategies to minimize cognitive side effects with ECT: aspects of ECT technique. J ECT. 2008
Mar. 24(1):46­51. [Medline].

82. Sackeim HA, Prudic J, Fuller R, Keilp J, Lavori PW, Olfson M. The cognitive effects of electroconvulsive
therapy in community settings. Neuropsychopharmacology. 2007 Jan. 32(1):244­54. [Medline].

83. Gardner BK, O'Connor DW. A review of the cognitive effects of electroconvulsive therapy in older adults. J
ECT. 2008 Mar. 24(1):68­80. [Medline].

84. Lyons JE, Symon J. Asystole during electroconvulsive therapy in an elderly woman treated concomitantly
with venlafaxine. Aust N Z J Psychiatry. 2008 Mar. 42(3):255. [Medline].

85. Holak EJ, Scott JP, Pagel PS. Electroconvulsive therapy­induced asystole: occurrence after 39 previous
uneventful treatments. Can J Anaesth. 2007 Sep. 54(9):772­3. [Medline].

86. White PF, Purdue L, Downing M, Thornton L. Intranasal sumatriptan for prevention of post­ECT
headaches. Headache. April 2006. 46(4):692. [Medline].

87. Suzuki K, Takano T, Ebina Y, Takamatsu K, Awata S, Matsuoka H. Continuation electroconvulsive therapy
to prevent relapse of schizophrenia in relapse­prone patients. J ECT. 2007 Sep. 23(3):204­5. [Medline].

88. Kellner CH, Knapp RG, Petrides G, et al. Continuation electroconvulsive therapy vs pharmacotherapy for
relapse prevention in major depression: a multisite study from the Consortium for Research in
Electroconvulsive Therapy (CORE). Arch Gen Psychiatry. 2006 Dec. 63(12):1337­44. [Medline].

89. Sackeim HA, Haskett RF, Mulsant BH, et al. Continuation pharmacotherapy in the prevention of relapse
following electroconvulsive therapy: a randomized controlled trial. JAMA. 2001 Mar 14. 285(10):1299­307.
[Medline].

90. Navarro V, Gasto C, Torres X, et al. Continuation/maintenance treatment with nortriptyline versus
combined nortriptyline and ECT in late­life psychotic depression: a two­year randomized study. Am J
Geriatr Psychiatry. 2008 Jun. 16(6):498­505. [Medline].

91. van den Broek WW, Birkenhager TK, Mulder PG, Bruijn JA, Moleman P. Imipramine is effective in
preventing relapse in electroconvulsive therapy­responsive depressed inpatients with prior pharmacotherapy
treatment failure: a randomized, placebo­controlled trial. J Clin Psychiatry. 2006 Feb. 67(2):263­8.
[Medline].

92. Dombrovski AY, Mulsant BH, Haskett RF, Prudic J, Begley AE, Sackeim HA. Predictors of remission after
electroconvulsive therapy in unipolar major depression. J Clin Psychiatry. 2005 Aug. 66(8):1043­9.
[Medline].

93. Fink M, Rush AJ, Knapp R, et al. DSM melancholic features are unreliable predictors of ECT response: a
CORE publication. J ECT. 2007 Sep. 23(3):139­46. [Medline].

94. Rasmussen KG, Mueller M, Knapp RG, et al. Antidepressant medication treatment failure does not predict
lower remission with ECT for major depressive disorder: a report from the consortium for research in
electroconvulsive therapy. J Clin Psychiatry. 2007 Nov. 68(11):1701­6. [Medline].

95. Fenton L, Fasula M, Ostroff R, Sanacora G. Can cognitive behavioral therapy reduce relapse rates of
depression after ECT? a preliminary study. J ECT. 2006 Sep. 22(3):196­8. [Medline].

Medscape Reference © 2011 WebMD, LLC